Başkaya M K, Rao A M, Prasad M R, Dempsey R J
Division of Neurosurgery, University of Kentucky Medical Center, Lexington, USA.
Neurosurgery. 1996 Jan;38(1):140-5. doi: 10.1097/00006123-199601000-00033.
This study examined ornithine decarboxylase (ODC) activity and edema formation bilaterally in brain cortices and hippocampi after lateral controlled cortical-impact injury in rats. To measure the activity of ODC, the brains of injured and control rats were frozen in situ at 30 minutes and at 6, 24, and 72 hours after controlled cortical-impact injury of moderate severity. The specific gravity of these regions was examined in decapitated animals at corresponding time points as an indicator of edema formation. Thirty minutes after injury, ODC activity did not increase in the injury-site cortex and ipsilateral hippocampus. At 6 hours after injury, ODC activity had increased by nine times that of the control in the injury-site cortex, by five times in the adjacent cortex, and by five and one-half times in the ipsilateral hippocampus. Twenty-four hours after injury, ODC activity had increased by three times that of the control in the injury-site cortex and two times in the ipsilateral hippocampus. Seventy-two hours after injury, activity had returned to control levels. ODC activity increased significantly in the contralateral cortex and hippocampus only at 6 and 24 hours. The injury-site and adjacent cortices and the ipsilateral hippocampus showed significant edema at 6, 24, and 72 hours but not at 30 minutes after injury. These findings indicate that polyamine metabolism is significantly altered in traumatic brain injury. The temporal association between ODC activity and edema formation indicates that polyamines might be a contributing factor in edema formation after traumatic brain injury. The delayed induction of ODC after brain injury suggests a potential therapeutic window for future pharmacological intervention to decrease posttraumatic secondary cerebral injury.
本研究检测了大鼠侧方控制性皮质撞击伤后双侧大脑皮质和海马中鸟氨酸脱羧酶（ODC）的活性及水肿形成情况。为测定ODC活性，在中度严重程度的控制性皮质撞击伤后30分钟、6小时、24小时和72小时，将受伤大鼠和对照大鼠的大脑原位冷冻。在相应时间点，对断头动物的这些区域的比重进行检测，作为水肿形成的指标。损伤后30分钟，损伤部位皮质和同侧海马中的ODC活性未增加。损伤后6小时，损伤部位皮质中的ODC活性增加至对照的9倍，相邻皮质增加5倍，同侧海马增加5.5倍。损伤后24小时，损伤部位皮质中的ODC活性增加至对照的3倍，同侧海马增加2倍。损伤后72小时，活性恢复至对照水平。仅在6小时和24小时时，对侧皮质和海马中的ODC活性显著增加。损伤部位和相邻皮质以及同侧海马在损伤后6小时、24小时和72小时出现明显水肿，但在损伤后30分钟未出现。这些发现表明，创伤性脑损伤中多胺代谢发生了显著改变。ODC活性与水肿形成之间的时间关联表明，多胺可能是创伤性脑损伤后水肿形成的一个促成因素。脑损伤后ODC的延迟诱导提示了未来药物干预以减少创伤后继发性脑损伤的潜在治疗窗。
